
Motor unit plasticity is defined as the ability of motoneurons and their respective muscles to change physically and functionally due to activity, age, and other factors. Timing is an important factor in motor plasticity, as evidenced by studies on reward timing and its effect on motor learning. The timing of rewards during motor training can alter the learning dynamics and the consolidation of new motor memories. Diffusion MRI studies have also revealed the dynamic nature of learning-induced plasticity, with different plasticity patterns emerging when feedback on timing is provided. Furthermore, spike-timing-dependent plasticity highlights the importance of temporal order in conveying and storing information in neuronal circuits. The timing of stimuli can influence the strengthening or weakening of connections between nerve cells. Overall, the role of timing in motor plasticity is a critical aspect that requires further exploration to enhance our understanding of brain function and develop effective rehabilitation programs.
| Characteristics | Values |
|---|---|
| Motor unit plasticity | The ability of motoneurons and their respective effector muscles to physically and functionally change as a result of activity, age, and other factors |
| Neural plasticity | The brain adapts, compensates, and learns throughout life |
| Enriched environments | Environments that provide a variety of stimulating activities and social interactions |
| Maladaptive plasticity | Can trigger behavioral changes or development of disease symptoms as a result of neurophysiological changes in the brain |
| Firing frequency | Defined as the number of neuronal signals sent per second on one motoneuron; maximum firing frequency in humans typically ranges from 100 to 200 Hz |
| EMG amplitude | The measure of the electric potential of motor units; maximum EMG amplitude is commonly referred to as maximum neuronal output |
| Spike-timing-dependent plasticity (STDP) | A change in synaptic strength based on the difference in firing time of pre- and post-synaptic neurons |
| Tau-coupling theory | The perception of temporal information (intrinsic or extrinsic) guides the timing of our movements |
| Pre-performance routines | Extrinsic temporal information that can improve the outcome of an action |
| Prospective information | Information about the current future, i.e., where we are going and how we will get there |
| Rate-based plasticity | High-frequency presynaptic stimulation induces long-term potentiation (LTP), while low-frequency stimulation induces long-term depression (LTD) |
| Dopamine | Required for normal STDP in the basal ganglia; dopamine depletion can contribute to motor learning deficits |
| Inhibitory long-term plasticity | Requires retrograde signaling and neuromodulators, such as endocannabinoid release and activation of presynaptic M2 muscarinic acetylcholine receptors |
| Motor learning deficits | Associated with STDP disruption and dopamine loss in PD models and patients |
| Motor recovery | Enriched environments and physical activity facilitate motor recovery and increase neural plasticity |
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What You'll Learn

Motor unit plasticity and resistance training
Motor unit plasticity refers to the ability of motoneurons and their respective muscles to change physically and functionally due to activity, age, and other factors. Motoneurons are a type of neuron that communicates with acetylcholine receptors on the motor end plate of the effector muscle, causing its contraction.
Motor unit plasticity is important for improving athletic performance and preventing age-related immobility. Resistance training, for instance, has been shown to improve the performance of larger muscle groups, which is crucial for athletes in high-impact and fast-paced sports.
The impact of resistance training on motor unit plasticity can be measured in several ways, with neural firing frequency being the most significant. Firing frequency is the rate at which neuronal signals are sent per second to a motoneuron, and it is measured in Hertz. Resistance training can increase this frequency by up to 40% in professional athletes. This increase in frequency improves athletic performance by reducing the time to maximum muscle contraction, or reaction time, rather than increasing maximum force output.
EMG amplitude, or electromyography, is another important measure of motor unit plasticity. It assesses the electric potential of motor units, with higher amplitudes indicating greater neuronal output. Resistance training has been shown to increase EMG amplitude, with gains ranging from minimal to 50% after just one month of training. However, consistent and repetitive training may lead to a plateau in amplitude increases, requiring variation in the training regimen to further enhance muscular force.
Other methods for measuring motor unit plasticity include muscle force output, pre-synaptic inhibition, and synchronization. While force output increases with resistance training, it typically plateaus after a month of consistent practice. To further improve force output, variation in training load or repetition is necessary. Additionally, studies have shown that resistance training increases nerve terminal branching, which is indicative of pre-synaptic plasticity. However, physical activity does not seem to increase the number of acetylcholine receptors on the effector muscle, and inactivity decreases them.
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Motor impairment and maladaptive plasticity
Compensatory movements can improve performance in daily activities, but they can also induce maladaptive plasticity and hinder motor recovery. For example, a patient with hemiparesis may bear more weight on the opposite lower extremity, leading to asymmetry and impaired posture. The non-affected extremity compensates for the paretic limb, but this compensation can result in postural imbalance.
Several mechanisms contribute to maladaptive plasticity:
- Compensatory movements: As mentioned earlier, compensatory movements involve the adaptation of remaining motor elements or substitution of functions to different body parts. While this can maximize functional ability in the short term, it can also lead to inappropriate movement patterns that limit normal motor patterns and hinder motor recovery.
- Changes to ipsilateral motor projections: Ipsilateral motor projections are usually weak in an undamaged nervous system. After a stroke, these projections are activated to compensate for the loss of contralateral motor projections. However, they are often unable to sufficiently support the disruption of corticospinal motor projections, leading to abnormal movement and poor motor ability.
- Competitive interaction between hemispheres: The competitive interaction between the damaged and undamaged hemispheres of the brain can induce abnormal interhemispheric inhibition, weakening motor function. This widespread disinhibition increases the risk of competitive interaction between the hand and proximal arm, resulting in incomplete motor recovery.
It is important to note that maladaptive plasticity is not limited to stroke patients. For instance, resistance training can increase the maximum firing frequency of motoneurons, improving athletic force and reaction time. However, it does not increase the maximum force output of a single motor unit, and the effects plateau after about a month of consistent training.
In summary, motor impairment and maladaptive plasticity are interconnected, particularly in the context of stroke recovery and athletic performance. While the brain's plasticity allows for compensation and adaptation, it can also lead to negative consequences such as maladaptive plasticity, hindering motor recovery and potentially causing further impairment. Understanding these mechanisms is crucial for developing effective rehabilitation programs that minimize maladaptive plasticity and promote motor recovery.
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Enriched environments and stroke recovery
Enriched environments are a multi-faceted form of housing that provides enhanced motor, cognitive, sensory, and social stimulation. These environments are designed to be stimulating and enriching for animals, closely mimicking conditions encountered in the wild.
Following a stroke, an enriched environment can aid recovery by creating a neural environment that is conducive to healing, resulting in improved cognitive and gross motor function. This is achieved through neuroplasticity, the ability of the brain to change its structure and function in response to new environments or injuries. Enriched environments have been shown to increase neuroplasticity, thereby improving functional recovery after a stroke. Animal studies have demonstrated that post-stroke animals in enriched environments exhibit better functional recovery, including improved motor function and cognitive performance, compared to those in standard housing.
The benefits of enriched environments are not limited to animal studies. Social interaction, for instance, has been shown to positively impact post-stroke recovery in humans. Living with a healthy partner has been associated with enhanced benefits for stroke recovery. Furthermore, music therapy has been found to improve speech-motor coordination, resulting in better phonation, articulation, and resonance. Playing music with strong rhythms can excite motor neurons, leading to natural and ideal muscle movements. Music therapy has also been shown to enhance finger movements, upper extremity function, and gait, aiding in motor rehabilitation.
However, there are challenges to implementing enriched environments in human stroke rehabilitation. One of the main obstacles is the difficulty in standardizing enriched environment conditions across different clinical sites. Additionally, there is a lack of consensus on the critical components of enriched environments that are responsible for enhancing brain plasticity. Nevertheless, enriched environments show promise in promoting functional recovery after a stroke, and further research is being conducted to facilitate their transition into the clinical setting.
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Spike-timing-dependent plasticity (STDP) and Hebbian synaptic plasticity
The phenomenon of spike-timing-dependent plasticity (STDP) was initially observed in neuronal cultures and cortical slices. When a postsynaptic spike follows synaptic depolarization, the synapse develops long-term potentiation (LTP). Conversely, when a postsynaptic spike is followed by synaptic excitation, the implicated synapse undergoes long-term depression (LTD). STDP is a temporally asymmetric form of Hebbian learning, induced by tight temporal correlations between the spikes of pre- and postsynaptic neurons. It is widely believed that STDP underlies learning and information storage in the brain, as well as the development and refinement of neuronal circuits during brain development.
In its canonical form, STDP is temporally asymmetric: the causal pairing of pre- and postsynaptic spikes induces LTP, while the reversed, acausal ordering leads to LTD. The modification in synaptic efficacy depends on the causal relationship between the pre- and postsynaptic spikes. This is often referred to as an extension of Hebb's rule to the temporal domain.
Hebbian synaptic plasticity depends on the temporal order of activity between pre- and postsynaptic cells. In Hebbian theory, repeated and persistent activation of a presynaptic neuron contributes to the firing of a postsynaptic neuron, strengthening the connection between them. This principle is often summarised as "cells that fire together, wire together".
STDP provides specificity and competition at the level of individual synapses, while homeostatic plasticity provides stability and global regulation. Together, they enable learning in a dynamic environment. STDP finds and reinforces temporal patterns, while homeostatic and heterosynaptic processes prevent these changes from destabilising the neuron.
The STDP learning window differs across brain regions and cell types. While many synapses exhibit an asymmetric window favoring LTP for pre-before-post timing and LTD for post-before-pre timing, other synapses display symmetric, anti-Hebbian, or frequency-dependent patterns, especially under different neuromodulatory conditions or in inhibitory circuits. The activity requirements of STDP vary not only across brain regions and synapse types but also within a cell, in different dendritic compartments.
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Motor timing and tau-coupling theory
Motor timing is a concept that involves controlling the timing of our actions. This is something we do thousands of times a day without thinking, such as controlling our eyes to read or reaching out to pick up a cup.
The tau-coupling theory, or tau-coupling hypothesis, is a control theory that relates to motor timing. It proposes that moving targets are intercepted at a specified goal zone by maintaining a constant ratio between the tau (time to closure) of the gap between the hand and the goal zone and the tau of the gap between the hand and the moving target. In other words, the way the movement changes over time (the movement τ–τm) are linked to the perception of the dynamic temporal information (the informational τ–τ-guide [τi]). The dynamic temporal information prescribes the temporal course of the movement so that the information and movement are coupled in such a way that τm=kτi (where k is a constant representing the volitional control of movement).
However, the tau-coupling hypothesis has been criticised for ignoring neuronal delays. It is unclear how the tau of the gap between the hand and the target can be kept proportional to the tau of the gap between the target and the goal zone, as it takes time to determine the value of tau, send the appropriate motor commands to the muscles, and allow the muscles to contract. Therefore, it has been suggested that an implementation of tau-coupling in the brain would only be possible if future values of tau were predicted.
Research has been conducted to investigate whether the tau-coupling theory is a valid control strategy for interception in general. For example, one study modelled smooth ballistic hand movements that were independent of the target's movement but led to successful interception. The results showed that the relationship between the two decreasing taus could not be considered as evidence for the tau-coupling theory. Another study investigated the audiovisual guidance of movement in interceptive action using the tau-coupling model. The findings revealed that while the auditory contribution to movement guidance changed across conditions, the visual contribution remained constant, suggesting that tau-coupling can be used to disentangle the relative contributions of different sensory modalities in movement planning.
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Frequently asked questions
Motor unit plasticity is the ability of motoneurons and their respective muscles to physically and functionally change as a result of activity, age, and other factors.
Timing plays a crucial role in motor plasticity, particularly in the context of spike-timing-dependent plasticity (STDP). STDP refers to changes in synaptic strength based on the timing of pre- and postsynaptic neuron firing. The specific timing of spikes can lead to either synaptic strengthening (LTP) or weakening (LTD), influencing the overall plasticity of the neural circuit.
Motor unit plasticity is influenced by various factors, including physical activity, age, and training techniques. Resistance training, for example, has been shown to increase neural firing frequency and improve athletic performance.
Environments that offer a variety of stimulating activities, known as enriched environments, have been found to facilitate motor recovery and increase neural plasticity after a stroke. These environments provide greater opportunities for physical activity, social interaction, and cognitive engagement, promoting brain plasticity and recovery.
Timing is integral to motor performance, as it allows us to successfully interact with our dynamic environment. Our brains use perceptual information to control the timing of our actions, ensuring we act ahead of time and avoid potential collisions or unwanted outcomes. This understanding of timing is crucial for elite athletes and can be enhanced through preperformance routines that provide extrinsic temporal information.











































